目的:探讨CMTM5(CKLF—likeMARVE Ltransmembrance domain containing)对人前列腺癌裸鼠移植瘤的抑制作用,并初步探索其作用机制。方法:13只雄性裸鼠连续腹腔注射环磷酰胺2.5mg/(d·只),建立裸鼠皮下前列腺移植瘤模型,3周后11只裸鼠种植部位可见肿瘤,随机将其分成两组:实验组(6只),对照组(5只)。实验组肿瘤局部注射CMTM5腺病毒,对照组不作处理。每日监测裸鼠体重和肿瘤大小,2周后处死。取出完整肿瘤组织,利用免疫组化方法检测过表达CMTM5对裸鼠前列腺移植瘤组织中血管内皮生长因子(VEGF)及核转录因子KB(NF—κB)蛋白表达的影响。结果:CMTM5组肿瘤体积为(573.39±175.24)mm3明显小于对照组(1482.50±327.86)mm3,P=0.03。CMTM5组肿瘤重量为(0.55±0.11)g明显小于对照组(1.31±0.29)g,P=0.027。免疫组化法检测结果显示,与对照组比较,CMTM5组VEGF和NF-κB蛋白的表达明显降低。结论:CMTM5抑制前列腺癌的生长,其作用机制可能通过下调与肿瘤细胞增殖密切相关的血管内皮生长因子VEGF和核转录因子NF—κB的表达相关。
Objective: To investigate the inhibitory effect of CKLF-like MARVEL transmembrance domain containing 5 (CMTM5) on xenografted human prostatic cancer in nude mice and its action mechanism. Methods: We established a model of xenografted prostatic cancer by inoculating PC-3 cells subcutaneously into nude mice, and 3 weeks later injected CMTM5 adenovirus locally into the tumor followed by daily observation of the tumor volume and body weight of the experimental animals. All the rats were killed 2 weeks after CMTM5 injection and the tumor tissue harvested for detection of the inhibitory effect of CMTM5 on the expressions of VEGF and NF-κB proteins by immunohistochemistry. Results : The tumor volume was significantly smaller and body weight of the CMTM5-treated mice were (573.39 ± 175.24 ) mm3 and (0.55 ± 0.11 ) g, respectively, significantly decreased as compared with those of the controls ( [ 1482.50 ± 327.86 ] mm3 and [ 1.31 ± 0. 29 ] g) (P = 0.03 and P = 0. 027). Immunohistochemistry showed that the expressions of VEGF and NF-κB were obviously down-regulated in the CMTM5 group in comparison with the control group. Conclusion : CMTM5 suppresses the growth of prostate cancer by down-regulating the expressions of VEGF and NF-κB. Natl J An- drol, 2012, 18 (3) : 195 -199